NEURO-ONCOLOGY神经肿瘤学
NEURO-ONCOLOGY(英文缩写 NEURO-ONCOLOGY),ISSN 1522-8517,eISSN 1523-5866,中文译名:神经肿瘤学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-28 至 2026-09-28，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 13.029 | Q1 |
| 2022 | 15.900 | Q1 |
| 2023 | 16.400 | Q1 |
| 2024 | 13.400 | Q1 |
| 2025 | 13.100 | Q1 |
NEURO-ONCOLOGY 最新收录文献
-
1. Association of high tumor mutational burden with brain metastases: Insights from a large-scale database analysis.
PMID:日期:2026-09-26Brain metastases (BrM) are a major cause of cancer-related mortality. To successfully colonize the brain, cancer cells must acquire unique adaptations. We hypothesized that BrM, regardless of their primary tumor origin, share convergent molecular features enabling brain colonization while retaining tumor type-specific alterations. We analyzed genomic data from 150,486 tumor samples, including BrM (N = 4,538), non-brain metastases (non-BrM, N = 43,844), and local biopsies (LB, N = 71,738) across six cancer types: non-small cell lung cancer (NSCLC), colorectal cancer (CRC), breast cancer (BC), esophageal cancer, melanoma, and neuroendocrine tumors (NET). We compared genomic alterations (GA), pathway enrichment, high tumor mutation burden (TMB-high), and high microsatellite instability (MSI-H) across groups. Our research revealed that BrM were enriched for TMB-high and exhibited higher median values across all cancer types studied, compared to both LB and non-BrM. Interestingly, MSI-H, despite its known association with TMB-high, was not significantly enriched in BrM. We further showed a consistent enrichment of GA in TP53 in BrM across multiple tumor types. KRAS mutations were enriched in NSCLC and CRC BrM, while GA in TERT were specific to melanoma BrM. Pathway analysis showed that BrM have a higher frequency of GA in genes associated with the ERK-MAPK pathway and, to a lesser extent, the DNA damage response pathway. BrM harbor both tumor-specific and shared molecular traits, particularly TMB-high and recurrent TP53/KRAS alterations, potentially reflecting essential adaptations for BrM. These insights provide a molecular framework for developing targeted therapeutic strategies to prevent or treat BrM.
-
2. Cancer Neuroscience: Establishing a home in Neuro-Oncology.
PMID:日期:2026-09-25Although neurons innervate all organs in which solid tumors grow, the role of neurons in cancer biology has long been neglected. Over the past decade, numerous studies have elucidated the critical role of the nervous system in cancer pathophysiology, culminating in the birth of Cancer Neuroscience. The recognition that neurons dictate many aspects of tumor biology not only provides new opportunities for therapeutic targeting of these stromal dependencies but also underscores the strong bi-directional relationships between tumors and the nervous system that result in cancer-associated symptomatology. By recognizing the key place of neurons in tumor biology, Cancer Neuroscience has ushered in a new era in which brain cancers should be conceptualized as diseases of dysregulated neurodevelopment, neuroplasticity, and neurophysiological function, usurped to drive brain cancer growth, progression, and therapeutic resistance. Likewise, the nervous system governs the initiation, growth, spread, and survival of most (if not all) extracranial cancers, while also mediating communication from cancers to the brain. Herein, we outline the current state of Cancer Neuroscience and the roles for neuro-oncologists in this new aspect of cancer care as an introduction to an upcoming series of articles in Neuro-Oncology on cellular interactions in the healthy nervous system and in the setting of cancer.
-
3. Glioma and ependymoma through the lens of brain development, stem cells, and plasticity.
PMID:日期:2026-09-25Brain tumors are increasingly understood as having components of a development organization in which malignant cells leverage neural progenitor programs, lineage hierarchies, and circuit interactions that normally shape the developing brain. This review examines how these principles inform the biology of ependymoma and gliomas across the age spectrum, including H3 K27-altered diffuse midline glioma, H3 G34-mutant diffuse hemispheric glioma, IDH-mutant glioma, and glioblastoma. We highlight how tumor identity reflects developmental timing, regional context, and cell-of-origin competence, while also emphasizing that malignant cells can acquire plasticity beyond their normal counterparts. Across entities, single-cell, spatial, lineage-tracing, and organoid studies reveal progenitor-like compartments that sustain tumor growth, generate heterogeneous malignant states, and interact dynamically with the neural and immune microenvironment. Cancer neuroscience further extends this developmental framework by showing that neuronal activity, synaptic input, and neuromodulatory signaling can regulate tumor proliferation, migration, epigenetic state, and therapeutic response. Together, these findings argue that brain tumors should be viewed not as disorganized cellular masses but as aberrant developmental systems. Defining the developmental dependencies and circuit vulnerabilities of malignant progenitor states may enable more precise therapies that target tumor biology while preserving essential brain function.
-
4. Impact of [18F]FET-PET on MRI-Based Radiotherapy Target Volumes in Newly Diagnosed Glioblastoma:Results from the FET-PET in Glioblastoma (FIG) Study TROG 18.06.
PMID:日期:2026-09-24The FET-PET in Glioblastoma (FIG) study (TROG 18.06) assessed the impact of adding FET-PET to MRI on radiotherapy gross tumor volume delineation in newly diagnosed glioblastoma. This multicenter prospective phase 2 study evaluated participants with newly diagnosed glioblastoma IDH-wildtype undergoing post-operative MRI and FET-PET imaging before adjuvant radiotherapy, delivered according to standard MRI-based planning. The FET-PET-positive biological tumor volume (BTV) was used to derive the Hybrid (FET-PET+MRI) gross tumor volume (Hybrid-GTV). Primary outcomes were: 1) BTV excluded from the GTV defined on MRI alone (MR-GTV); 2) Hybrid-GTV excluded from the MR-GTV with both comparisons analyzed by non-overlap volume (cm3 and %), dosimetry (D98 and V95) and spatial similarity metrics; 3) clinically meaningful change in GTV non-overlap percentage volume with the addition of FET-PET. There were 172 participants recruited, n = 140 evaluable. Median BTV was 23.1 cm3, median MR-GTV was 32.1 cm3, and median Hybrid-GTV was 46.0 cm3. Hybrid-GTV was significantly larger than the MR-GTV (p < 0.001), with a larger Hybrid-GTV observed in 83% of cases. Comparing BTV to MR-GTV, median non-overlap volume was 10.1 cm3 and non-overlap percentage volume 53.5%. Comparing Hybrid-GTV to MR-GTV, median non-overlap volume was 14.9 cm3 and non-overlap percentage volume 33.9%. D98 and V95 were lower for the Hybrid-GTV than for the MR-GTV, suggesting lower dose coverage. Applying a > 20% non-overlap percentage volume threshold, 76% of participants had a meaningful change in GTV with the addition of FET-PET. FET-PET differed significantly from MRI-based GTV delineation, with its incorporation leading to a clinically meaningful change in GTV in the majority of participants.
-
5. Potentially inappropriate care at the end of life in patients with glioblastoma: A single-center observational cohort study.
PMID:日期:2026-09-23Timely integration of palliative care is critical in the management of patients with glioblastoma. This study evaluated the frequency and determinants of potentially inappropriate care in the final 3 months of life on population level. Patient characteristics and healthcare utilization were extracted from medical records for deceased patients diagnosed with glioblastoma, who survived at least 3 months after diagnosis and received routine care at a single tertiary hospital between January 2015 and February 2026. Potentially inappropriate care was defined as the proportion of patients with any of these indicators in the final 3 months of life: ≥2 emergency department visits, ≥2 hospital admissions, >14 consecutive hospitalization days, intensive care unit admission, chemotherapy administration, or in-hospital death. Logistic regression analyses were performed to identify factors associated with receiving potentially inappropriate care. The cohort included 310 patients (median age 66 [IQR 56-72], 60% male), of whom 22% (n = 67/310) received potentially inappropriate care in the final 3 months of life. Chemotherapy was the main driver (n = 58/67, 87%), followed by ≥2 hospital admissions (n = 10/67, 15%) and in-hospital death (n = 9/67, 13%). Older patients (OR 0.97, 95% CI, 0.94-0.99) or those with an unmethylated O6-methylguanine-DNA methyltransferase (MGMT) promoter (OR 0.42, 95% CI, 0.23-0.75) were less likely to receive potentially inappropriate care. One in 5 patients with glioblastoma received potentially inappropriate care at the end of life, predominantly through chemotherapy. Younger patients and those with methylated MGMT promoters were most affected. Identification of patients at risk may support targeted palliative care interventions.
-
6. Plasma proteomics for prognostic stratification in newly diagnosed primary central nervous system lymphoma.
PMID:日期:2026-09-23Baseline biomarkers anticipating outcome in primary central nervous system lymphoma (PCNSL) are limited, and classical scores rely on clinical variables alone. We present a plasma proteomic framework for prognostic stratification of newly diagnosed PCNSL. Baseline plasma from 162 newly diagnosed PCNSL patients (French LOC network; training n=84; test n=78) was profiled using Olink Reveal (1,007 proteins). Consensus k-means clustering applied to the training proteome was projected to the test cohort, evaluated for immune-signature enrichment, and assessed by multivariable Cox regression. An elastic-net classifier predicted early treatment failure, evaluated by held-out and nested cross-validated AUC. Clustering identified 2 proteomic states, Inflamed and Non-inflamed plasma, that replicated in the test cohort. The Inflamed state was enriched for pre-specified immune signatures, most strongly an Innate/Inflammatory signature. High Innate/Inflammatory scores marked shorter overall (OS) and progression-free survival (PFS) in training (log-rank P=.0014 OS, P=.0037 PFS) and test (P=5.4×10⁻⁴ OS, P=.0014 PFS), remaining significant after adjustment for MSKCC class and sex (test OS HR 2.51, P=.0022). Combining signatures with clinical variables improved test discrimination, most clearly for PFS (C-index 0.68 vs. 0.60). A supervised classifier predicted early treatment failure (PFS < 9 months) at test AUC 0.71, driven by the immune signatures rather than a whole-proteome search. Plasma proteomics identifies a reproducible Inflamed state in PCNSL associated with shorter OS and PFS that improves discrimination beyond clinical scores and stratifies the risk of early treatment failure. These findings support prospective evaluation of a focused innate-inflammatory plasma panel for risk stratification.
-
7. Immune Cell Engager Therapy for Brain Cancer.
PMID:日期:2026-09-18Improving outcomes for patients with brain tumors remains a formidable challenge. Patient survival is often considered very poor even though standard first line treatments include surgery, radiotherapy, and chemotherapy. These therapies often have detrimental side effects on brain functions and do not suffice when tumors advance and metastasize, prompting the need for new treatment modalities. Recent innovations in antibody-based immunotherapies may complement brain cancer treatment. Biotechnical engineering platforms yield new antibody-inspired biomolecules for optimal engagement of specific and tumor-associated antigens, which also recruit and elicit immune effector cell functions. Here, we review current advances on multi-specific immune cell engagers for brain tumor treatment and provide novel insights into overcoming existing challenges.
-
8. Murine modeling of IDH-mutant 1p/19q-codeleted oligodendroglioma reveals genotype specific phenotypes.
PMID:日期:2026-09-17Oligodendroglioma is a primary central nervous system tumor classified by the presence of isocitrate dehydrogenase (IDH) mutations and codeletion of 1p/19q. A lack of faithful preclinical model systems for this disease has limited progress in understanding the biology of this genetically unique subtype of adult diffuse-type glioma and in developing new effective therapies. To address this unmet need, we sought to establish a mouse model that faithfully recapitulates the genetic and phenotypic features of human IDH-mutant 1p/19q-codeleted oligodendroglioma. We performed in utero electroporation to introduce distinct combinations of genetic alterations and evaluated their potential to form tumors. Resulting tumors were characterized by histology, metabolite profiling, RNA-sequencing and single-cell RNA sequencing. We identified co-expression of IDH1R132H and PIK3CAE545K together with loss of Cic, Fubp1 and Cdkn2a (termed OligoCdkn2a) as the optimal genetic combination to drive fully penetrant tumors that histologically resemble human grade II/III IDH-mutant 1p/19q-codeleted oligodendroglioma. Substituting Cdkn2a loss with Trp53 deletion decreased latency and shifted tumors toward high-grade astrocytoma histology. OligoCdkn2a tumors displayed metabolic and transcriptional changes associated with IDH and CIC mutations, and single-cell sequencing identified a bias towards oligodendrocyte differentiation compared to an IDH wild-type glioblastoma mouse model. To our knowledge, OligoCdkn2a tumors represent the first autochthonous, genetically engineered mouse model to recapitulate the genetic, histological and transcriptional features of human IDH-mutant 1p/19q-codeleted oligodendrogliomas. This model will provide a valuable platform to further dissect mechanisms of tumorigenesis and test novel therapeutic strategies for this molecularly distinct glioma subtype.
-
9. Beyond Dose Escalation in Glioblastoma: Lessons Learned from INTRAGO-II and the Case for Targeting Tumor Biology.
PMID:日期:2026-09-17该文献暂无摘要。
-
10. High-grade astrocytoma with piloid features: a clinical and genomic analysis of prognostic factors using a large cohort.
PMID:日期:2026-09-16High-grade astrocytoma with piloid features (HGAP) is a recently defined tumor type that is not well-understood. Prognostic factors of clinical outcomes are not well-established. Methylation profiling was performed on tumor samples, many at the National Cancer Institute (NCI) Laboratory of Pathology, and others from publicly available sources. Methylation classifier scores of ≥ 0.90 to the HGAP class on the NCI-Bethesda classifier version 3 were included. Clinical features were collected from the medical record. Survival analyses were performed using the Kaplan-Meier and Cox-proportional hazards methods. The cohort comprised 421 patients. There were high rates of ATRX alteration (62%), CDKN2A/B homozygous loss (78%) and MGMT promoter methylation (53%). MAPK alterations were identified in 74% of evaluable samples. The median age was 46 years, and posterior fossa location was predominant (52%). The median overall survival (OS) was 88 months. Older age (p = 0.01) and the presence of an ATRX alteration (p = 0.04) were found to be negative prognostic factors. The presence of cystic features on magnetic resonance imaging (MRI) was found to be favorably prognostic (p = 0.01). Factors that were not significantly associated with prognosis included histologic high-grade features, CDKN2A/B homozygous deletion, MGMT promoter methylation, extent of resection, and presence of NF1 syndrome. This large cohort establishes relative frequencies of several important markers. Additionally, older age, the presence of an ATRX alteration, and cystic features on MRI were found to be prognostic. Our work may aid in optimizing treatment regimens for patients with this tumor type.